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Expression of a bovine growth hormone transgene inhibits pregnant mare's serum gonadotropin-induced follicle maturation in prepuberal gilts

Author:
Guthrie, H.D., Pursel, V.G., Bolt, D.J., Cooper, B.S.
Source:
Journal of animal science 1993 v.71 no.12 pp. 3409
ISSN:
0021-8812
Subject:
gilts, somatotropin, pregnant mare serum gonadotropin, follicular fluid, gene expression, androstenedione, progesterone, inhibin, transgenic animals, ovarian follicles
Abstract:
Prepuberal gilts were injected with PMSG to determine whether expression of a bovine growth hormone (bGH) transgene inhibited preovulatory maturation of ovarian follicles. Seven transgenic (TG) gilts of line 3706, which expresses a mouse metallothionein-bGH transgene, and eight nontransgenic, control (C) gilts (128 to 147 d old) were injected with PMSG, 12.5 IU/kg BW, 72 h before necropsy. Surface ovarian follicles > 1 mm in diameter were counted, measured for diameter, and aspirated for fluid. Follicles were classified morphologically as healthy or atretic and those with follicular fluid estradiol-17 beta > 100 ng/mL were classified as estrogen-active (EA). The number of follicles per gilt was 64.3 +/- 6.1 (mean +/- SEM) and did not differ significantly between bGH-TG and C gilts. The PMSG treatment induced growth of large (> 5 mm) follicles in both bGH-TG and C gilts. However, compared with C gilts, bGH-TG gilts had fewer (P <.05) large follicles (5.9 +/- 1.5 vs 18.3 5.4), a lower proportion of EA large follicles (35 +/- 12.5 vs 69 +/- 13.2%), and in large follicles less (P < .05) estradiol-17 beta (86 +/- 17 vs 350 +/- 69 ng/mL) and androstenedione (300 +/- 33 vs 1,283 +/- 221 ng/mL). Follicular fluid progesterone and inhibin did not differ significantly between bGH-TG and C gilts. The incidence of atresia among small and medium follicles did not differ significantly between bGH-TG and C gilts. These results indicate that chronic, unregulated expression of a bGH transgene in prepuberal gilts inhibited follicle growth in response to administration of PMSG and may have blocked estradiol-17 beta production in vivo by inhibiting theca interna androgen production.
Agid:
33888
Handle:
10113/33888